Long term learning disabilities and other behavioral deficits have been described in children who were exposed to ethanol prenatally. A disorganization of neuronal and glial elements observed in the brains of such children and in animal models of ethanol exposure in utero may explain these learning and behavioral deficits. The hippocampal formation, an area of the brain involved with learning and memory, is quite sensitive to the effects of ethanol both pre- and postnatally. Anatomic and behavioral studies of fetal alcohol animals suggest a functional deficit within the hippocampal formation of these animals. The neurochemical manifestation(s) of this proposed functional deficit are unknown. The experiments outlined in this proposal are designed to study neurotransmitter receptors and several other neurochemical parameters in the hippocampal formation of animals exposed to ethanol prenatally. Attention will be focused on the dentate granule cells, their efferent projection to the hippocampal CA3-4 pyramidal cells and the afferent inputs to dentate granule cells. Using radiohistochemical techniques, the number and distribution of glutamate, muscarinic cholinergic, serotonergic, noradrenergic, GABA, kappa-opiate and adenosine receptors will be examined in the hippocampal formation of fetal alcohol animals and compared to ad lib fed and pair fed controls. The disposition of zinc in the axonal terminals of dentate granule cells after an intraventricular injection of zinc65 will also be examined. Finally, three neurochemical parameters will be examined that are thought to be associated with the mechanisms of long term potentiation in the hippocampal formation, and possibly with learning. The experiments described in this proposal should provide considerable information regarding the effects of ethanol exposure in utero on the hippocampal formation.